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HYPERKALAEMIA TALK AND A LITTLE HYPOKALAEMIA BY DR NIHAL ABOSAIF CONSULTANT ACUTE PHYSICIAN.

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Presentation on theme: "HYPERKALAEMIA TALK AND A LITTLE HYPOKALAEMIA BY DR NIHAL ABOSAIF CONSULTANT ACUTE PHYSICIAN."— Presentation transcript:

1 HYPERKALAEMIA TALK AND A LITTLE HYPOKALAEMIA BY DR NIHAL ABOSAIF CONSULTANT ACUTE PHYSICIAN

2 OBJECTIVES OF THE TALK 1- TO UNDERSTAND THE CAUSES OF HYPERKALAEMIA 2- TO KNOW HOW TO DIFFERENTIATE BETWEEN THE SEVERITY OF CASES OF HYPERKALAEMIA 3- TO KNOW HOW TO MANAGE HYPERKALAEMIA AND HYPOKALAEMIA 4- TO UNDERSTAND SOME OF THE PATHOPHYSIOLOGY BEHIND DIFFERENT SCENARIOS 5- IDENTIFY SOME CAUSES OF HYPOKALAEMIA AND HOW TO DEAL WITH THEM.

3 PHYSIOLOGY  POTASSIUM IS ONE OF THE BODY'S MAJOR IONS.  NEARLY 98% OF THE BODY ’ S POTASSIUM IS INTRACELLULAR.  THE RATIO OF INTRACELLULAR TO EXTRACELLULAR POTASSIUM IS IMPORTANT IN DETERMINING THE CELLULAR MEMBRANE POTENTIAL.  SMALL CHANGES IN THE EXTRACELLULAR POTASSIUM LEVEL CAN HAVE PROFOUND EFFECTS ON THE FUNCTION OF THE CARDIOVASCULAR AND NEUROMUSCULAR SYSTEMS.  THE KIDNEY DETERMINES POTASSIUM HOMEOSTASIS, AND EXCESS POTASSIUM IS EXCRETED IN THE URINE.

4  potassium is necessary for the maintenance of normal charge difference between intracellular and extracellular environments.  potassium homeostasis is tightly regulated by specific ion-exchange pumps (primarily by a cellular, membrane-bound, sodium-potassium ATP-ase).  Derangements of potassium regulation often lead to neuromuscular, gastrointestinal, and cardiac conduction abnormalities. INTRODUCTION

5 CASE 1 SCENARIO 55 YR OLD MALE WITH KNOWN TYPE 2 DM, HTN, HYPERCHOLESTEROLAEMIA AND IHD PRESENTED WITH INCREASED SOB, CHEST TIGHTNESS, MILD CONFUSION AND TACHYCARDIA. HE DEVELOPED URINARY FREQUENCY, DYSURIA AND CLOUDY URINE FOR THE LAST COUPLE OF DAYS. HE NORMALLY TAKES PERINDOPRIL 5MG OD, ASPIRIN 75MG OD, FUROSEMIDE 40MG OD, SIMVASTATIN 40MG NOCT, BISOPROLOL 5MG OD AND AMLODIPINE 5MG OD.

6 EXAMINATION; BP 170/100, HR 95/M, RR 26/M, SATS 95% AND T 36.7C CHEST; BILATERAL FINE BASAL CRACKLES HEART AND ABDOMEN NAD BLOODS: S.CREAT 250MMOL/L, S.BUN 20, S.K 6.5, S.NA 140 LFTS, FBC NAD CRP 25 ABG; PH 7.25, PCO2 3.5, PO2 10, HCO3 15, BE -7, LACT 1.5 CASE 1 SCENARIO

7 ECG

8 MANAGEMENT WHAT’S WRONG WITH THIS PATIENT WHAT’S YOUR FIRST PRIORITY FIRST LINE THERAPY 2 ND LINE MAINTENANCE TREATMENT

9 MANAGEMENT- CASE 1 1-ACUTE ON CHRONIC RENAL FAILURE CORRECT POTASSIUM LEVEL BY GIVING ONE DOSE OF CALCIUM GLUCONATE 10MG AMPOULE INSULIN DEXTROSE STOP NEPHROTOXIC MEDICATIONS IVI (BE WARE OF LV FUNCTION) TREAT UNDERLYING CAUSE; UTI, RENAL ACIDOSIS, REFER TO RENAL PHYSICIANS FOR F/U

10 CASE 2 SCENARIO 75 ELDERLY GENTLEMAN WITH KNOWN BPH AND MILD HTN PREVIOUSLY FIT AND WELL BECAME VERY CONFUSED OVER LAST 3 DAYS THEN WAS UNABLE TO PASS URINE FOR THE LAST 12 HOURS WITH DULL ACHING PAIN IN THE SUPRAPUBIC REGION WIFE CALLED GP TO SEE PATIENT BUT SUDDENLY HE BECAME UNRESPONSIVE AND VERY BREATHLESS.

11 CASE 2 SCENARIO EXAMINATION; BP 70/40, HR 35/M, RR 30/M, SATS 85% AND T 36.7C CHEST; NAD HEART AND ABDOMEN NAD BLOODS: S.CREAT 800MMOL/L, S.BUN 50, S.K 8.5, S.NA 140 LFTS, FBC NAD CRP 45 ABG; PH 7.05, PCO2 2.5, PO2 20, HCO3 5, BE -17, LACT 9

12 ECG-1

13 ECG 2

14 MANAGEMENT WHAT’S WRONG WITH THIS PATIENT WHAT’S YOUR FIRST PRIORITY FIRST LINE THERAPY 2 ND LINE MAINTENANCE TREATMENT

15 MANAGEMENT- CASE 2 IMMEDIATE MANAGEMENT OF HYPERKALAEMIA AS LIFE THREATENING GET ITU IMMEDIATELY IV CALCIUM CHLORIDE OR CALCIUM GLUCONATE UP TO 50 MG INSTANTEOUSLY UNTIL ECG CHANGES IV INSULIN DEXTROSE IV SODIUM BICARBONATE NEBS WHEN SLIGHTLY BETTER URGENT DIALYSIS AFTER STABILISATION

16 POSSIBLE CAUSE IS RENAL OBSTRUCTION, ? STONE, MASS OR ENLARGED PROSTATE URGENT USS KUB TO R/O HYDRONEPHROSIS NEPHROSTOMY RENAL AND UROLOGY RV MANAGEMENT- CASE 2

17 CASE 3 SCENARIO 25 YEAR OLD FEMALE WITH IDDM PRESENTED WITH DIARRHOEA AND VOMITING. SHE WAS UNABLE TO KEEP ANY FLUIDS IN AND BECAME VERY DEHYDRATED. SHE DIDN’T HAVE HER INSULIN DOSES FOR THE LAST 24HOURS AS SHE FELT VERY TIRED AND LETHARGIC. ON ARRIVAL TO A&E, SHE LOOKED VERY DEHYDRATED, SOB AND VOMITED TWICE IN RESUS.

18 CASE 3 SCENARIO EXAMINATION; BP 80/50, HR 125/M, RR 26/M, SATS 95% OA AND T 36.7C CHEST; CLEAR HEART AND ABDOMEN NAD BLOODS: S.CREAT 110MMOL/L, S.BUN 20, S.K 7.0, S.NA 120 LFTS, FBC WBCS 15, N 13, HB 15 CRP 35 ABG; PH 7.02, PCO2 2.5, PO2 11, HCO3 15, BE -8, LACT 5

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20 MANAGEMENT WHAT’S WRONG WITH THIS PATIENT WHAT’S YOUR FIRST PRIORITY FIRST LINE THERAPY 2 ND LINE MAINTENANCE TREATMENT

21 MANAGEMENT- CASE 3 HYPERKALAEMIA IS SECONDARY TO DKA INSULIN DEFICIENCY CAUSED SHIFT OF K FROM IC COMPARTMENT TO EC COMPARTMENT TREATMENT IS BY CORRECTING DKA AS IN PROTOCOL IVI 1,2,4, 6 HOURLY BAGS OF IV N SALINE FIXED RATE INSULIN CHECK ABG HOURLY IF K STARTS TO BE LOW THEN START GLUCOSE 5% AND K INFUSION

22 CASE 4 SCENARIO 43 YEAR OLD WOMAN RETURNED FROM A TRIP TO CYPRUS WITH SEVERE D&V. SHE WAS PREVIOUSLY FIT AND WELL WITH NO MEDICAL ILLNESSES. SHE WAS TRYING TO DRINK AS MUCH AS SHE CAN BUT KEPT ON HAVING RUNNING THROUGH DIARRHOEA. SHE FEELING VERY TIRED AND LETHARGIC AFTER THREE DAYS THEN WASN’T ABLE TO MOVE HER LOWER LIMBS

23 CASE 4 SCENARIO ON EXAMINATION, BP 90/60, HR 45/M, RR 12/M, SATS 95% OA AND T 37.7C CHEST AND HEART; CLEAR ABDOMEN, SOFT BUT TENDER AND DISTENDED AND SLUGGISH BOWEL SOUNDS NEURO: POWER 1/5 IN BOTH LL, NO SENSORY LOSS OR SPEECH CN LOSS. MILD DYSPHAGIA BLOODS: S.CREAT 120MMOL/L, S.BUN 20, S.K 2.0, S.NA 120 LFTS, FBC WBCS 15, N 13, HB 10 CRP 150 ABG; PH 7.5, PCO2 5.5, PO2 9, HCO3 28, BE +3, LACT 3

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25 MANAGEMENT WHAT’S WRONG WITH THIS PATIENT WHAT’S YOUR FIRST PRIORITY FIRST LINE THERAPY 2 ND LINE MAINTENANCE TREATMENT

26 MANAGEMENT- CASE4 HYPOKALAEMIA SECONDARY TO D&V PARALYSIS SECONDARY TO HYPOKALAEMIA TREATMENT; IV POTASSIUM INFUSION THROUGH A CENTRAL LINE RATE MMOL/HOUR IVI

27 UNDERSTANDING CAUSES HYPERKALEMIA IS MOST OFTEN DUE TO DECREASED URINARY POTASSIUM EXCRETION SECONDARY TO ACUTE OR CHRONIC KIDNEY DISEASE AND/OR DISORDERS OR DRUGS THAT INHIBIT THE RAAS. LESS COMMONLY, TOTAL BODY POTASSIUM CAN REMAIN THE SAME OR EVEN DECREASE AND POTASSIUM CAN MOVE OUT OF THE CELLS SECONDARY TO VARIOUS PROCESSES (SUCH AS HYPERGLYCEMIA). THIS RESULTS IN REDISTRIBUTIVE HYPERKALEMIA.

28 INDICATIONS FOR TREATMENT HYPERKALEMIA PER LAB RESULTS WITH ECG CHANGES PRESENT SERUM POTASSIUM GREATER THAN 6.5 TO 7 MMOL/L A SERUM POTASSIUM THAT IS RAPIDLY INCREASING – NOTE HERE THAT IN PATIENTS WITH SUBSTANTIAL TISSUE BREAKDOWN (EG, RHABDOMYOLYSIS, CRUSH INJURY, TUMOR LYSIS SYNDROME) LARGE AMOUNTS OF POTASSIUM IS RELEASED FROM THE CELLS, WHICH CAN LEAD TO RAPID AND SUBSTANTIAL ELEVATIONS IN SERUM POTASSIUM. SO AGGRESSIVE TREATMENT IS INDICATED EVEN WITH ONLY SLIGHT INCREASE IN POTASSIUM PER SERUM STUDIES.

29 ESSENTIALLY THE TREATMENT COMES DOWN TO ACUTELY MANAGING HYPERKALEMIA AND ITS ADVERSE RESULTS AND THEN ULTIMATELY REMOVING EXCESS POTASSIUM IF THE SITUATION CALLS FOR IT. – THIS CAN BE BROKEN DOWN IN TO THREE APPROACHES TO THE TREATMENT 1) ANTAGONIZING THE MEMBRANE EFFECTS OF POTASSIUM – USING CALCIUM 2) DRIVING EXTRACELLULAR POTASSIUM INTO THE CELLS – INSULIN WITH GLUCOSE, BETA-2-ADRENERGIC AGONISTS AND SODIUM BICARBONATE 3) REMOVING EXCESS POTASSIUM FROM THE BODY – DIURETICS, RESINS OR DIALYSIS

30 MECHANISM OF ACTION OF CALCIUM MECHANISM: DIRECTLY ANTAGONIZES THE MEMBRANE ACTIONS OF HYPERKALEMIA. HIGH LEVELS OF POTASSIUM INDUCE DEPOLARIZATION OF THE RESTING MEMBRANE POTENTIAL WHICH LEADS TO INACTIVATION OF SODIUM CHANNELS AND DECREASED MEMBRANE EXCITABILITY. THIS LEADS TO THE CARDIOTOXICITY OF HYPERKALEMIA. THIS IS A POTENTIALLY FATAL COMPLICATION OF HYPERKALEMIA SO CALCIUM TX IS VERY IMPORTANT EARLY IN SEVERE CASES. – ONSET: EFFECT OF IV CALCIUM IS SEEN WITHIN MINUTES AND LASTS FOR MINUTES. – INDICATIONS: SEVERE MANIFESTATIONS WITH WIDE QRS COMPLEXES OR LOSS OF P WAVES. ESSENTIALLY IN PATIENTS WHERE IT IS TOO RISKY TO WAIT THE 30 MINUTES TO AN HOUR IT TAKES OF INSULIN TO PROVIDE BENEFITS. – EFFECT: PROTECTS HEART BUT DOES NOT CHANGE SERUM POTASSIUM LEVELS. – DOSE: CALCIUM GLUCONATE 1000 MG OVER 2-3 MINUTES. CALCIUM CHLORIDE 500 TO 1000 MG OVER 2-3 MINUTES. CENTRAL ACCESS PREFERRED WITH CALCIUM CHLORIDE DUE TO POSSIBLE PERIPHERAL VEIN IRRITATION AND EXTRAVASATION LEADING TO TISSUE NECROSIS. REPEAT EITHER AFTER 5 MINUTES IS EKG CHANGES PERSIST. – SPECIAL NOTE: IN PATIENTS BEING TREATED WITH DIGITALIS CALCIUM SHOULD BE ADMINISTERED MORE SLOWLY AND WITH A MORE DILUTE SOLUTION. THIS IS TO AVOID CARDIOTOXIC EFFECTS OF CALCIUM THAT PATIENTS ON DIGITALIS ARE SUSCEPTIBLE TO.

31 SHIFT OF K INTRACELLULARY DEXTROSE- INSULIN MECHANISM: INSULIN ENHANCES THE ACTIVITY OF THE NA-K-ATPASE PUMP IN SKELETAL MUSCLE THUS DRIVING POTASSIUM IN TO THE CELLS AND REDUCING SERUM CONCENTRATIONS. GLUCOSE IS GIVEN TO PREVENT HYPOGLYCEMIA BUT IS NOT NEEDED IF BLOOD GLUCOSE IS ABOVE 20 MMOL/L – ONSET: EFFECT OF INSULIN BEGINS IN 10 TO 20 MINUTES BUT DOES NOT PEAK UNTIL 30 TO 60 MINUTES. THE EFFECTS LAST FOR 4-6 HOURS. – EFFECT: UP TO 0.85 MMOL/L DECREASE IN POTASSIUM IN ONE HOUR. – DOSE: EITHER DRIP OR BOLUS. DRIP IS 10 UNITS OF REGULAR INSULIN IN 500 ML OF 10% DEXTROSE OVER 60 MINUTES. BOLUS IS 10 UNITS OF REGULAR INSULIN FOLLOWED BY 50ML OF 50% DEXTROSE. BOLUS REGIMEN PROVIDES A BETTER REDUCTION IN SERUM POTASSIUM DUE TO HIGHER INSULIN LEVELS ACHIEVED BY BOLUS BUT THERE IS A HIGHER INCIDENCE OF HYPOGLYCEMIA IN PATIENTS RECEIVING BOLUS THERAPY. – SPECIAL NOTE: GIVING GLUCOSE ALONE THEORETICALLY RAISES ENDOGENOUS INSULIN LEVELS PROVIDING A THERAPEUTIC EFFECT BUT ENDOGENOUS RELEASE IS HIGHLY VARIABLE. IF ENDOGENOUS INSULIN RELEASE IS IMPAIRED, HYPERGLYCEMIA CAN RESULTS WHICH WILL ACTUALLY RAISE PLASMA OSMOLALITY PROMOTING WATER AND POTASSIUM MOVEMENT OUT OF CELLS AND WORSEN HYPERKALEMIA.

32 BETA 2 AGONISTS ESSENTIALLY THIS IS EITHER ALBUTEROL (OR SALBUTAMOL) OR EPINEPHRINE. ALBUTEROL IS USED RARELY AND EPINEPHRINE SHOULD REALLY NOT BE USED AT ALL. EPINEPHRINE ALSO HAS ALPHA-ADRENERGIC ACTIVITY WHICH CAN ACTUALLY CAUSE POTASSIUM MOVEMENT OUT OF CELLS, NOT INTO THEM. – MECHANISM: LIKE INSULIN ALBUTEROL INCREASES THE ACTIVITY OF THE NA-K-ATPASE PUMP IN SKELETAL MUSCLE. IN ADDITION IT ALSO ACTIVATES THE NA-K-2CL COTRANSPORTER. BOTH ACT TO DRIVE POTASSIUM INTO CELLS. – ONSET: PEAK EFFECT IS 90 MINUTES WITH NEBULIZATION AND 30 MINUTES WHEN GIVEN IV. – EFFECT: HAS BEEN SHOWN TO LOWER POTASSIUM CONCENTRATIONS BY 0.5 TO 1.5 MMOL/L.

33 SODIUM BICARBONATE MECHANISM: RAISES THE SERUM PH RESULTING IN HYDROGEN ION RELEASE FROM CELLS TO BUFFER. THIS H RELEASE IS ACCOMPANIED BY POTASSIUM MOVEMENT INTO CELLS TO MAINTAIN ELECTRONEUTRALITY – ONSET: WITHIN 15 MINUTES VIA IV WITH DURATION OF ACTION OF 1-2 HOURS. – INDICATIONS: LIMITED EVIDENCE SUPPORTING THE ACUTE MANAGEMENT OF HYPERKALEMIA WITH SODIUM BICARBOANTE. IT SHOULD NOT BE USED ALONE IN ACUTE THERAPY BUT CAN BE BENEFICIAL IN CHRONIC KIDNEY DISEASE PATIENTS WITH METABOLIC ACIDOSIS REGARDLESS OF POTASSIUM. – DOSE: IN ACUTE SETTING (AGAIN NOT AS MONOTHERAPY) SHOULD BE GIVEN AS 150 MMOL IN 1L OF D5W. IF GIVEN IN NORMAL SALINE YOU ARE GIVING INCREASED SODIUM SO PLASMA OSMOLALITY WILL INCREASED AND SLOW THE CORRECTION OF HYPERKALEMIA

34 OTHER MODALITIES; DIALYSIS DIALYSIS IS THE ULTIMATE TX IF ALL OTHER MODALITIES HAVE FAILED OR THE HYPERKALEMIA IS EXTREMELY SEVERE OR INCREASING RAPIDLY. – HEMODIALYSIS IS PREFERRED OVER PERITONEAL DIALYSIS. – HEMODIALYSIS CAN REMOVE 25 TO 50 MMOL OF POTASSIUM/ HOUR

35 HYPOKALAEMIA

36 DEFINITION HYPOKALEMIA IS DEFINED AS A POTASSIUM LEVEL LESS THAN 3.5 mmol/h.HYPOKALEMIA IS DEFINED AS A POTASSIUM LEVEL LESS THAN 3.5 mmol/h. MODERATE HYPOKALEMIA IS A SERUM LEVEL OF mmol/h.MODERATE HYPOKALEMIA IS A SERUM LEVEL OF mmol/h. SEVERE HYPOKALEMIA IS DEFINED AS A LEVEL LESS THAN 2.5 mmol/hSEVERE HYPOKALEMIA IS DEFINED AS A LEVEL LESS THAN 2.5 mmol/h THE REFERENCE RANGE FOR SERUM POTASSIUM LEVEL IS mmol/h

37 PATHOPHYSIOLOGY Total body deficit of potassium Acute potassium depletion potassium shifts from the EC to IC space Other causes chronic inadequate intake, long-term diuretic or laxative use, chronic diarrhea, hypomagnesemia & hyperhidrosis diabetic ketoacidosis, severe GI losses : vomiting / diarrhea, dialysis, and diuretic therapy Alkalosis & hypothermia insulin, catecholamines Distal RTA & Bartter syndrome, Periodic hypokalemic paralysis, Hyperaldosteronism & hyperthyroid.

38 ABNORMALITIES OF SERUM POTASSIUM ARE ASSOCIATED WITH WELL DESCRIBED CLINICAL FEATURES: S. K+ level Clinical features <3.5 mmol/l Lassitude < 2.5 mmol/l Possible muscle necrosis <2 mmol/l Flaccid paralysis with respiratory compromise Gennari FJ. Hypokalemia. N Engl J Med 1998; 339:

39 EFFECTS OF HYPOKALEMIA ATRIAL/VENTRICULAR ARRHYTHMIAS ARE MORE COMMON IN PATIENTS WITH UNDERLYING HEART DISEASE (ESPECIALLY CAD) AND IN PATIENTS TAKING DIGOXIN. LIFE-THREATENING CARDIAC ARRHYTHMIAS CAN OCCUR WHEN THE SERUM POTASSIUM IS VERY LOW (< 2 MEQ/L), OR WHEN THE SERUM POTASSIUM IS RELATIVELY LOW (2 - 3 MEQ/L) IN PATIENTS WITH UNDERLYING HEART DISEASE, OR WHEN THE PATIENT IS DIGOXIN-TOXIC.

40 SEVERE (OR RAPIDLY OCCURRING) HYPOKALEMIA CAN CAUSE MUSCLE WEAKNESS AND PARALYSIS THE PARALYSIS MAINLY AFFECTS THE PROXIMAL LOWER EXTREMITIES => PROGRESSING TO AFFECT THE UPPER EXTREMITIES; DYSPHAGIA AND DYSARTHRIA ARE UNCOMMON AND CRANIAL NERVE PALSIES ARE EXCEEDINGLY RARE) RHABDOMYOLYSIS CAN OCCUR IN SEVERELY POTASSIUM- DEPLETED PATIENTS - ESPECIALLY FOLLOWING VIGOROUS EXERCISE - AND MUSCLE NECROSIS CAN RARELY OCCUR EFFECTS OF HYPOKALEMIA

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42 IV INFUSION RATE FOR SEVERE OR SYMPTOMATIC HYPOKALEMIA Standard IV replacement rate Standard IV replacement rate mmol/h Serum potassium < 2.5 meq/L, or Serum potassium < 2.5 meq/L, or Moderate-severe symptoms Moderate-severe symptoms mmol/h Serum potassium < 2.0 Meq/L, or Serum potassium < 2.0 Meq/L, or Life-threatening symptoms Life-threatening symptoms > 40 mmol/h If heart block, or If heart block, or Renal insufficiency exists Renal insufficiency exists mmol/h

43 Transient, asymptomatic, or mild hypokalemia may resolve spontaneously or may be treated with enteral potassium supplements. Potassium replacement therapy is immediately indicated for: mmol/h  Severe hypokalemia (< 2.5 mmol/h ), or  If the hypokalemia is causing muscle paralysis, or  Malignant cardiac arrhythmias. Medical Decision-Making and Treatment

44 MEDICAL DECISION-MAKING AND TREATMENT  OUTPATIENT THERAPY AND FOLLOW-UP IN HOURS MAY BE ACCEPTABLE FOR MILD HYPOKALAEMIA PATIENTS WITH NO UNDERLYING HEART DISEASE.

45 THE PATIENT SHOULD BE TRANSFERRED TO ICU FOR SEVERE OR SYMPTOMATIC HYPOKALEMIA FOR:  IV POTASSIUM SUPPLEMENTATION.  CONTINUOUS CARDIAC MONITORING. MEDICAL DECISION-MAKING AND TREATMENT

46 MAGNESIUM REPLACEMENT THERAPY MAGNESIUM REPLACEMENT THERAPY IS OFTEN NECESSARY IN MALNOURISHED ALCOHOLICS WITH HYPOKALEMIA. HYPOMAGNESEMIA SHOULD BE SUSPECTED IF THE SERUM POTASSIUM DOES NOT INCREASE WITHIN ~ 72 HOURS OF THE COMMENCEMENT OF POTASSIUM SUPPLEMENTATION THERAPY. MAGNESIUM CAN BE GIVEN ORALLY (3G X 4 DOSES).

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